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- W2130764511 abstract "See related article, p 80–87Endogenous glucocorticoids have long been recognized to play a pivotal role in orchestrating an adaptive response of the host to stress, from trauma and infection to inflammation. Therefore, it is not surprising that glucocorticoids received considerable attention as potential therapeutic agents for acute myocardial infarction. Numerous studies documented their ability to protect the heart from ischemia-reperfusion injury in many animal and in vitro models.1 However, clinical trials with glucocorticoids for the treatment of acute myocardial infarction have yielded inconsistent results, with both a small beneficial effect on mortality and adverse influence on longer term remodeling being reported.2 A likely explanation for these discrepant observations is that the benefits of local anti-inflammatory actions of glucocorticoids in the ischemic heart are offset by adverse systemic effects. Thus, understanding of the mechanisms underlying local protective actions of glucocorticoids is of particular importance. In most cell types, glucocorticoids suppress prostaglandin biosynthesis that contributes to dampening of inflammation. By contrast, glucocorticoids were found to upregulate cycloxoygenase-2 expression in rodent cardiomyocytes and exert cytoprotective effects via activation of lipocalin-type prostaglandin D (PGD) synthase–mediated PGD2 synthesis.3 However, PGD2 receptors and downstream signaling pathways have not been characterized in this study.In this issue of Hypertension , Katsumata et al4 fill this important gap in our knowledge by demonstrating that the cardioprotective actions of endogenous PGD2 are mediated predominantly through activation …" @default.
- W2130764511 created "2016-06-24" @default.
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- W2130764511 date "2014-01-01" @default.
- W2130764511 modified "2023-09-30" @default.
- W2130764511 title "Glucocorticoid Protection Against Myocardial Ischemia-Reperfusion Injury" @default.
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- W2130764511 doi "https://doi.org/10.1161/hypertensionaha.113.01832" @default.
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